Question

14. Describe three of the cognitive vulnerabilities associated with the development of depression. Include in your response evidence indicating the significant role distorted cognitive schemas play in developing a mood disorder. How would an individual at high risk for depression and one at low risk for depression differ in how they would think, say and act after a significant appointment (e.g., failing an exam, breakup of a relationship).

Answer 1

Depression is a substantial public health burden that shows dramatic increases from childhood into adolescence and adulthood. Rates of depression skyrocket from early to late adolescence (Hankin & Abela, 2005). Numerous etiological factors and processes have been proposed and studied to explain why individuals become depressed (Abela & Hankin, 2008a).

Cognitive theories of depression are prominent etiological models that have been extensively studied in adults and are increasingly being applied to account for the development of depression across the lifespan (Hankin & Abela).

In short, according to cognitive theories of depression, depressed and depression-vulnerable individuals are hypothesized to exhibit attention, interpretation, inferential, and memory biases for salient stimuli.

The most prominent cognitive theories include Beck’s cognitive theory (BT; Beck, 1987), hopelessness theory (HT; Abramson, Metalsky, & Alloy, 1989), and response styles theory (RST; Nolen-Hoeksema, 1991).

Each theory highlights different cognitive vulnerabilities and processes hypothesized to contribute to depression.

BT focuses on negative schema and dysfunctional attitudes, which are rigid and extreme cognitive structures that negatively filter and bias social and affective information.

HT emphasizes a negative cognitive style, which comprises negative inferences about the cause of events (i.e., negative attributional style), self-implications, and consequences that individuals make in response to events.

RST proposes rumination as a process of repeatedly focusing on symptoms of depression and the meaning, causes, and consequences of the symptoms.

Considerable evidence supports cognitive vulnerabilities from these main theories as prospective predictors of depression among adults, adolescents, and children.

Both dysfunctional attitudes from BT and a negative cognitive style from HT moderate the longitudinal association between stressors and depression, consistent with the cognitive vulnerability-stress hypothesis of these theories, and baseline rumination has been shown to predict prospective elevations of depression (see Abela & Hankin, 2008b; Hankin & Abela, 2005; Lakdawalla, Hankin, & Mermelstein, for reviews).

Despite considerable evidence supporting cognitive vulnerabilities and processes predicting depression, it is important to note that numerous factors and mechanisms contribute to the ontogeny of depression as it is a multifactorial disorder. As such, cognitive vulnerabilities are a contributory, but not a necessary, cause of depression, and so youth may become depressed without exhibiting cognitive vulnerability.

Given the successful predictive power of these central cognitive vulnerabilities in accounting for prospective increases in depression across the lifespan, investigators have increasingly turned attention to the potential developmental origins of these cognitive factors to understand when they emerge, consolidate, and stabilize into relatively enduring, trait-like risks to depression.

The primary focus of this article is to review evidence for some of the processes and factors that have been postulated to contribute to the emergence and stabilization of cognitive vulnerabilities. In particular, we focus on genetic factors, temperament, parenting and peers as salient interpersonal influences, and stressful events and contexts

Genetic Associations With Cognitive Vulnerabilities to Depression

Numerous studies have examined genetic influences on the development of depression, yet few have investigated associations between genes and cognitive vulnerabilities to depression. Hankin and Abramson (2001) hypothesized that genetic factors would operate as a distal risk to the development of cognitive vulnerabilities.

Since then, both behavioral and molecular genetic studies in the last few years have found evidence supporting the association between genes and several cognitive vulnerabilities to depression  

These studies provide initial evidence suggesting that cognitive vulnerabilities may function as possible endophenotypes, or intermediate risk factors, connecting the distal etiological risk of genetics to the phenotype of depression.

Temperament and its Relation to Depression and Cognitive Vulnerabilities

Individual temperamental traits, which are moderately heritable, are known to relate to depression in childhood and adolescence. Furthermore, temperament may play a role in the ontogeny of depression either directly or by increasing risk for the formation of cognitive vulnerabilities and other risk processes (Hankin & Abramson, 2001). T

hree major dimensions of temperament include negative emotionality (NE), positive emotionality (PE), and attentional control (AC; Compas, Connor-Smith, & Jasser, 2004). NE is conceptualized as an inclination toward experiencing intense discomfort, such as fear and anger, and reacting more easily to stress. PE is an inclination toward pleasure and reward from one’s environment. Last, AC is defined as the ability to control emotions, behaviors, and focus.

Origins and Stability of Cognitive Vulnerabilities: The Role of Interpersonal Factors

Cognitive vulnerabilities for depression may begin to stabilize during adolescence (Hankin & Abela, 2005), but research suggests that fluctuations can still occur together with stability (Hankin, 2008). Adolescence is a period in which interactions with peers begins to increase while relations with parents maintain importance (Steinberg & Morris, 2001). Therefore, parental influences may play a considerable role in the formation of cognitive vulnerabilities in childhood, whereas experiences with peers may strongly contribute to changes of these vulnerabilities during adolescence.

Very little research however has investigated the role of peers in the maintenance and exacerbation of cognitive vulnerabilities. Additionally, most of the evidence for parental influences is based on correlating self-reports of parent and child measures of cognitive vulnerabilities.

Although informative, observational studies are needed to elucidate which social factors are related specifically to different cognitive vulnerabilities and explicate the mechanisms through which these interpersonal influences may lead to the development and exacerbation of cognitive vulnerabilities over time.